Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/164367
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dc.contributor.authorTeh, Ye Cheanen_US
dc.contributor.authorChooi, Ming Yaoen_US
dc.contributor.authorLiu, Dehuaen_US
dc.contributor.authorKwok, Immanuelen_US
dc.contributor.authorLai, Ghee Chuanen_US
dc.contributor.authorOw Yong, Liyana Ayuben_US
dc.contributor.authorNg, Melissaen_US
dc.contributor.authorLi, Jackson L. Y.en_US
dc.contributor.authorTan, Yingrouen_US
dc.contributor.authorEvrard, Maximilienen_US
dc.contributor.authorTan, Leonarden_US
dc.contributor.authorLiong, Ka Hangen_US
dc.contributor.authorLeong, Keithen_US
dc.contributor.authorGoh, Chi Chingen_US
dc.contributor.authorChan, Andrew Y. J.en_US
dc.contributor.authorNurhidaya Binte Shadanen_US
dc.contributor.authorMantri, Chinmay Kumaren_US
dc.contributor.authorHwang, You Yien_US
dc.contributor.authorCheng, Huien_US
dc.contributor.authorCheng, Taoen_US
dc.contributor.authorYu, Weimiaoen_US
dc.contributor.authorTey, Hong Liangen_US
dc.contributor.authorLarbi, Anisen_US
dc.contributor.authorSt John, Ashleyen_US
dc.contributor.authorAngeli, Veroniqueen_US
dc.contributor.authorRuedl, Christianeen_US
dc.contributor.authorLee, Bernetten_US
dc.contributor.authorGinhoux, Florenten_US
dc.contributor.authorChen, Swaine L.en_US
dc.contributor.authorNg, Lai Guanen_US
dc.contributor.authorDing, Jeak Lingen_US
dc.contributor.authorChong, Shu Zhenen_US
dc.date.accessioned2023-01-18T01:13:43Z-
dc.date.available2023-01-18T01:13:43Z-
dc.date.issued2022-
dc.identifier.citationTeh, Y. C., Chooi, M. Y., Liu, D., Kwok, I., Lai, G. C., Ow Yong, L. A., Ng, M., Li, J. L. Y., Tan, Y., Evrard, M., Tan, L., Liong, K. H., Leong, K., Goh, C. C., Chan, A. Y. J., Nurhidaya Binte Shadan, Mantri, C. K., Hwang, Y. Y., Cheng, H., ...Chong, S. Z. (2022). Transitional premonocytes emerge in the periphery for host defense against bacterial infections. Science Advances, 8(9), eabj4641-. https://dx.doi.org/10.1126/sciadv.abj4641en_US
dc.identifier.issn2375-2548en_US
dc.identifier.urihttps://hdl.handle.net/10356/164367-
dc.description.abstractCirculating Ly6Chi monocytes often undergo cellular death upon exhaustion of their antibacterial effector functions, which limits their capacity for subsequent macrophage differentiation. This shrouds the understanding on how the host replaces the tissue-resident macrophage niche effectively during bacterial invasion to avert infection morbidity. Here, we show that proliferating transitional premonocytes (TpMos), an immediate precursor of mature Ly6Chi monocytes (MatMos), were mobilized into the periphery in response to acute bacterial infection and sepsis. TpMos were less susceptible to apoptosis and served as the main source of macrophage replenishment when MatMos were vulnerable toward bacteria-induced cellular death. Furthermore, TpMo and its derived macrophages contributed to host defense by balancing the proinflammatory cytokine response of MatMos. Consequently, adoptive transfer of TpMos improved the survival outcome of lethal sepsis. Our findings hence highlight a protective role for TpMos during bacterial infections and their contribution toward monocyte-derived macrophage heterogeneity in distinct disease outcomes.en_US
dc.description.sponsorshipAgency for Science, Technology and Research (A*STAR)en_US
dc.description.sponsorshipNational Research Foundation (NRF)en_US
dc.language.isoenen_US
dc.relationNRF2017_SISFP09en_US
dc.relation.ispartofScience Advancesen_US
dc.rights© 2022 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution NonCommercial License 4.0 (CC BY-NC).en_US
dc.subjectScience::Medicineen_US
dc.subjectScience::Biological sciencesen_US
dc.titleTransitional premonocytes emerge in the periphery for host defense against bacterial infectionsen_US
dc.typeJournal Articleen
dc.contributor.schoolLee Kong Chian School of Medicine (LKCMedicine)en_US
dc.contributor.schoolSchool of Biological Sciencesen_US
dc.contributor.organizationYong Loo Lin School of Medicine, NUSen_US
dc.contributor.organizationNational Skin Centreen_US
dc.contributor.organizationSingapore Immunology Network (SIgN), A*STARen_US
dc.identifier.doi10.1126/sciadv.abj4641-
dc.description.versionPublished versionen_US
dc.identifier.pmid35245124-
dc.identifier.scopus2-s2.0-85125790365-
dc.identifier.issue9en_US
dc.identifier.volume8en_US
dc.identifier.spageeabj4641en_US
dc.subject.keywordsBacterial Infectionsen_US
dc.subject.keywordsHost Defenseen_US
dc.description.acknowledgementThis research was funded by Singapore Immunology Network (SIgN) core funding and A*STAR, Singapore. F.G. is an EMBO YIP awardee and is supported by SIgN core funding and Singapore National Research Foundation Investigatorship (NRF2016NRF-NRF1001-02). L.G.N. is supported by SIgN core funding. S.Z.C. is supported by the Ministry of Health, Singapore’s National Medical Research Council under its Open Fund-Young Individual Research Grant (OFYIRG17may036), and A*STAR Career Development Award (192D8043). Y.C.T. is a graduate scholar supported by the Ministry of Education, Singapore. M.Y.C. is a graduate scholar supported by the SIgN-NTU-NUS scholarship, Singapore. SIgN Flow Cytometry facility is supported by National Research Foundation (NRF) Singapore under Shared Infrastructure Support (SIS) (NRF2017_SISFP09).en_US
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